Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103 ) is incorrect, any correction of the statutory basis for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
DETAILED ACTION
Claim status
Claims 45-58 are pending
Claims 45-58 are under examination
Information Disclosure Statement
The information disclosure statement (IDS) submitted on 2/06/2025 is in compliance with the provisions of 37 CFR 1.97. Accordingly, the information disclosure statement is being considered by the examiner.
However, Applicant is reminded that the listing of references in the specification is not a proper information disclosure statement. 37 CFR 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Examiner’s Comment
Applicant is reminded that an affidavit or declaration, such as those submitted under 37 CFR 1.130, 1.131 and 1.132, filed during the prosecution of the prior application do not automatically become a part of this application. Where it is desired to rely on an earlier-filed affidavit or declaration, the applicant should make the remarks of record in this application and include a copy of the original affidavit or declaration filed in the prior application (see MPEP 201.06, IX).
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The factual inquiries set forth in Graham v. John Deere Co., 383 U.S. 1, 148 USPQ 459 (1966), that are applied for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
Claims 45-48, 50, 54-56, and 58 are rejected under 35 U.S.C. 103 as being unpatentable over Kenderian et al. (US2021/0214723, filed 5/31/2019, published 7/15/2021), in view of Keck et al. (US2018/0187210, filed 12/21/2017, published 7/05/2018) and Shultz et al., (WO 2018/209344, filed 5/14/2018, published 11/15/2018)
In regard to claims 45 and 56, Kenderian teaches a patient derived xenograft (PDX) mouse model comprising
(i) engrafted human acute lymphoblastic leukemia (ALL) cells that express the cell surface tumor antigen CD19,
(ii/iii) human immune cells developed from peripheral blood mononuclear cells (PBMCs),
(iv) human cytokines such as IL-1 secreted from the human immune cells, and
(v) human immune chimeric antigen receptor (CART19) that specifically binds the cell surface antigen on the engrafted human tumor cells; wherein
([0020-0021, 0024-0026, 0085-0087, 0094-0095, 0099, 0101-103], Example 2, see Fig. 7D-E, Figs. 11-13). Note in regard to elements (ii/iii), although product-by-process claims are limited by and defined by the process, the method of production does not affect whether the product is novel or nonobvious. In instant case, Kenderian teaches “PMBCs” are administered, which naturally comprise a mixture of immune cells, and also allows the PMBCs to reside in the mouse model for nearly a month (10 days + 14 days) ([0020], Fig. 7D), which would naturally allow them to “develop” and/or differentiate into at least one immune cell (see Example 6 of Kenderian).
However, although Kenderian teaches the PDX xenograft first undergoes lymphodepletion with busulfan prior to administering the CART cells [0094-0095], they are silent with respect to irradiating the immunodeficient mouse prior to the administration of the CART cells and PMBCs.
In regard to claims 45 and 56, Keck teaches an immunodeficient mouse model comprising administered human immune cells and engrafted with a human tumor, wherein the immunodeficient mouse is subjected to radiation prior to administering the human immune cells ([0018, 0141-0143, 0155-0158, 0161], see Examples 2 & 3).
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing to prepare the immunodeficient mouse model comprising administered human CART cells and human PBMCs, wherein the immunodeficient mouse pretreated with the radiomimetic drug busulfan as taught by Kenderian, and substitute the radiomimetic drug with whole body radiation as taught by Keck with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Keck because whole body radiation prior to administering human immune cells is a form of conditioning that depletes or suppress the hematopoietic cells endogenous to the recipient prior to xenogeneic (i.e., human) cell administration [0108]. Furthermore, as stated supra, Keck teaches the busulfan is a radiomimetic, and that radiation was well known technique, thus the substitution of busulfan for the art recognized equivalent of whole body radiation would have been well within the level of ordinary skill in the art.
However, although Kenderian teaches the NSG strain for the xenograft, which corresponds to the NOD.Cg-Prkdcscid Il2rgtm1Wjl/SzJ genotype, they are silent to a mouse corresponding to the NOD.Cg-Prkdcscid H2-K1tm1Bpe H2-Ab1em1Mvw H2-D1tm1Bpe Il2rgtm1Wjl/SzJ, wherein NSG strain further comprises MHC Class I H2-K1, H2-D1, and H2-A genes knocked out (i.e., NSG-(Kb Db)null (IAnull) genotype).
In regard to instant claims 45 and 56, Shultz teaches an immunodeficient mouse model comprising administered human immune cells and engrafted with a human tumor, wherein the immunodeficient mouse is a NOD.Cg-Prkdcscid H2-K1tm1Bpe H2-Ab1em1Mvw H2-D1tm1Bpe Il2rgtm1Wjl/SzJ, which comprises MHC Class I H2-K1, H2-D1, and H2-A genes knocked out (i.e., NSG-(Kb Db)null (IAnull) genotype) (Abstract, [0013]).
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing to prepare the immunodeficient mouse model comprising administered human CART cells and engrafted with a human tumor as taught by Kenderian, and substitute the NOD.Cg-Prkdcscid H2-K1tm1Bpe H2-Ab1em1Mvw H2-D1tm1Bpe Il2rgtm1Wjl/SzJ mouse as the immunodeficient mouse as taught by Shultz with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Shultz because this particular strain of mouse allows a higher percentage of human IgG to remain in circulation over time ([0149, 0152], see Fig. 2 of Shultz). Thus, this mouse would be more appropriate for testing the humanized anti-GM-CSF antibodies in the methods of Kenderian (see [0149] of Shultz).
In regard to claims 46-48 and 50, as stated supra, Kenderian teaches anti-CD19 CAR engineered T cells, which were derived from a normal human donor [0028, 0070].
In regard to claims 54 and 58, Kenderian teaches the primary human ALL tumor cells derived from clinical patients while the PMBCs were derived from normal human donors [0075, 0086-0087], and thus were allogenic.
In regard to claim 55, as states supra, Kenderian teaches the macrophages developed from the PMBCs secreted IL-1 among other cytokines [0102].
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary
Claims 46-49 and 51 are rejected under 35 U.S.C. 103 as being unpatentable over Kenderian et al. (US2021/0214723, filed 5/31/2019) in view of Keck et al. (US2018/0187210, filed 12/21/2017, published 7/05/2018) and Shultz et al., (WO 2018/209344, filed 5/14/2018, published 11/15/2018), as applied to claim 45, in further view of Brusko et al. (PLoS ONE, 2010, 5(7))
As stated supra, Kenderian et al. suggest an immunodeficient NOD.Cg-Prkdcscid H2-K1tm1Bpe H2-Ab1em1Mvw H2-D1tm1Bpe Il2rgtm1Wjl/SzJ (i.e., NSG-(Kb Db)null(IAnull)) mouse model comprising administered human CART cells and PBMCs and immune cells developed therefrom, and engrafted with a human tumor, wherein the mouse further comprises human cytokines released from the human immune cells.
However, although Kenderian et al. teaches that the mouse model is to measure cytokine release syndrome (CRS) and neurotoxicity in the presence of CART cell therapy [0003], they are silent to combining TCR modified TREGs.
In regard to claims 46-49 and 51, Brusko teaches mouse tumor models comprising human TREGS genetically modified with a TCR in combination with antigen-sepcific T cell therapy of the tumor (Abstract, p. 2, Results).
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing to prepare an immunodeficient mouse tumor model comprising administered human CART, human PBMCs and engrafted with human tumor to study CRS and neurotoxicity as taught by Kenderian, and combine tumor antigen specific TREGS modified with a TCR as taught by Brusko with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Brusko because TCR-redirected TREGS are capable of suppressing the antigen-specific T cells in vivo, thereby generating antigen-specific tolerance by targeting the regulatory properties of TREGs to specific antigen targets (p. 6, Results, 1st para, p. 8, Discussion), which would be applicable to controlling the CRS and neurotoxicity in the PDX mouse model of Kenderian.
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
Claim 52 is rejected under 35 U.S.C. 103 as being unpatentable over Kenderian et al. (US2021/0214723, filed 5/31/2019) in view of Keck et al. (US2018/0187210, filed 12/21/2017, published 7/05/2018) and Shultz et al., (WO 2018/209344, filed 5/14/2018, published 11/15/2018), as applied to claims 45-48, in further view of Frank et al. (US2020/0299644, filed 2/08/2018, published 9/24/2020)
As stated supra, Kenderian et al. suggest an immunodeficient NOD.Cg-Prkdcscid H2-K1tm1Bpe H2-Ab1em1Mvw H2-D1tm1Bpe Il2rgtm1Wjl/SzJ (i.e., NSG-(Kb Db)null(IAnull)) mouse model comprising administered human CART cells and PBMCs and immune cells developed therefrom, and engrafted with a human tumor, wherein the mouse further comprises human cytokines released from the human immune cells.
However, Kenderian et al. are silent with respect to the CART cells being TILs.
Frank teaches compositions for T cell therapy of human tumors comprising administering human TILs comprising an engineered receptor that specifically binds to cell surface antigen on human cancer cells [0023-0024, 0093-0096, 0117-0119, 0292, 0333-0335, 0357-0359, 0402, 0416-0417].
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing to prepare an immunodeficient mouse model comprising administered human CART cells, human PBMCs, and engrafted with a human tumor as taught by Kenderian, and substitute TILs as the CART cells as taught by Frank with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Frank because compared to naïve T cells, TILs exhibit increased proliferation, migration, activation and anti-tumor efficacy [0004, 0159].
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
Claims 53 and 57 are rejected under 35 U.S.C. 103 as being unpatentable over Kenderian et al. (US2021/0214723, filed 5/31/2019, published 7/15/2021), in view of Keck et al. (US2018/0187210, filed 12/21/2017, published 7/05/2018) and Shultz et al., (WO 2018/209344, filed 5/14/2018, published 11/15/2018), as applied to claims 45 and 56, in further view of Holland et al. (Cell Tissue Bank, 2018, 19:783790)
As stated supra, Kenderian et al. suggest an immunodeficient NOD.Cg-Prkdcscid H2-K1tm1Bpe H2-Ab1em1Mvw H2-D1tm1Bpe Il2rgtm1Wjl/SzJ (i.e., NSG-(Kb Db)null(IAnull)) mouse model comprising administered human CART cells and PBMCs and immune cells developed therefrom, and engrafted with a human tumor, wherein the mouse further comprises human cytokines released from the human immune cells.
However, although Kenderian teaches the T cells can be obtained from patients to be treated [0049, 0052], they are silent with respect to the PBMCs and tumor cells being autologous.
Holland teaches PBMCs are essential to the study of autoimmune diseases and cancer, and describes compositions of banked human PBMCs from human patients with tumors (Abstract).
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing to prepare an immunodeficient mouse model comprising administered human CART cells, human PBMCs, and engrafted with a human tumor as taught by Kenderian, and choose PBMCs obtained from the human tumor patients as taught by Holland with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so not only because Holland suggest using immune cells from the same cancer patient, but as because Holland teaches that in the field of cancer immunology, the cellular phenotyping of a patients PMBCs provides critical information about patients responses to treatments (Abstract/Background, 1st para.), which would be applicable to the PDX mouse model of Kenderian.
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
Overcoming Rejection by Declaration under 37 CFR 1.130
Ye et al., (FASEB J, 2020, 9:12963-12975) appears to be Applicant’s own work. Applicant may rely on the exception under 35 U.S.C. 102(b)(1)(A) to overcome this rejection under 35 U.S.C. 102(a)(1) by a showing under 37 CFR 1.130(a) that the subject matter disclosed in the reference was obtained directly or indirectly from the inventor or a joint inventor of this application, and is therefore not prior art under 35 U.S.C. 102(a)(1) . Alternatively, applicant may rely on the exception under 35 U.S.C. 102(b)(1)(B) by providing evidence of a prior public disclosure via an affidavit or declaration under 37 CFR 1.130(b).
Claims 45-48, 50, 54-56, and 58 are rejected under 35 U.S.C. 103 as being unpatentable over Ye et al., (FASEB J, 2020, 9:12963-12975), in view of Kenderian et al. (US2021/0214723, filed 5/31/2019)
In regard to claims 45 and 56, Ye teaches a murine model comprising
an irradiated immunodeficient mouse comprising
(ii) human PMBCs to produce a humanized immunodeficient mouse engrafted with human PBMCs,
wherein the human PBMCs develop into human cells comprising T cells and B cells, Natural Killer cells and monocytes,
wherein the human cells secrete cytokines,
wherein the irradiated immunodeficient mouse is a NOD-Prkdcnull Il2rgnull H2-K1null H2-D1null H2-Ab1null genotype (alias NSG-MHC-DKO);
(c) measuring the levels of secreted human cytokines circulating in the humanized immunodeficient mouse.
However, although Ye teaches that immunotherapy with CAR-T cells for cancer is encompassed by therapy-related CRSs (Abstract, Introduction, 1st para.), Ye is silent to step (a)(i) administering human tumor cells to said mouse, and step (b) administering engineered human immune cells comprising a receptor specific for a human tumor cell antigen.
In regard to claims 45 and 56, Kenderian teaches a CAR T cell therapy-related cytokine release syndrome (CRS) in a murine model comprising
an immunodeficient mouse comprising
(i) human leukemia cells that express the CD19 tumor antigen,
(ii) human PMBCs to produce a humanized immunodeficient mouse
(b) administering engineered human anti-CD19 CART cells to the humanized immunodeficient mouse,
(c) measuring the levels of secreted human cytokines circulating in the humanized immunodeficient mouse ([0020-0021, 0024-0026, 0085-0087, 0094-0095, 0099, 0101-103], Example 2, see Fig. 7D-E, Figs. 11-13).
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing prepare the irradiated immunodeficient mouse comprising PBMCs as taught by Ye, and combine administered human CD19 cancer cells, and human anti-CD19 CART cells as taught by Kenderian with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so because Ye teaches that one of the therapies known to cause CRS is CART cell therapy, and using the humanized immunodeficient mouse of Ye to examine CRS base CART cell therapy would have an obvious extension of the teachings of Ye.
In regard to claims 46-48 and 50, as stated supra, Ye teaches that immunotherapy with CAR-T cells for cancer, and Kenderian teaches anti-CD19 CAR engineered T cells, which were derived from a normal human donor [0028, 0070].
In regard to claims 54 and 58, Kenderian teaches the primary human ALL tumor cells derived from clinical patients while the PMBCs were derived from normal human donors [0075, 0086-0087], which would have been a predictably obvious choice because of the ability to draw from banked cells (see [0075, 0086] of Kenderian).
In regard to claim 55, Ye teaches measuring the circulating levels of IL-6, IL-10, IFN-gamma, TNF, IL-2, and IL-4 (Figure 2). Furthermore, as stated supra, Kenderian measuring circulating cytokine/chemokine levels in the mouse blood after CART injection (Example 2).
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary
Claims 46-49 and 51 are rejected under 35 U.S.C. 103 as being unpatentable over Ye et al., (FASEB J, 2020, 9:12963-12975), in view of Kenderian et al. (US2021/0214723, filed 5/31/2019), as applied to claim 45, in further view of Brusko et al. (PLoS ONE, 2010, 5(7))
As stated supra, Ye in view of Kenderian suggest an irradiated immunodeficient mouse comprising administered human CART cells and PBMCs, and engrafted with a human tumor.
However, although both Ye and Kenderian et al. teaches that the mouse model is to measure cytokine release syndrome (CRS) in the presence of therapy (p. 12972, Discussion of Ye, see also [0003] of kenderian), they are silent to combining TCR modified TREGs.
In regard to claims 46-49 and 51, Brusko teaches mouse tumor models comprising human TREGS genetically modified with a TCR in combination with antigen-sepcific T cell therapy of the tumor (Abstract, p. 2, Results).
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing to prepare an immunodeficient mouse tumor model comprising administered human CART, human PBMCs and engrafted with human tumor to study CRS as taught by Ye in view of Kenderian, and combine tumor antigen specific TREGS modified with a TCR as taught by Brusko with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Brusko because TCR-redirected TREGS are capable of suppressing the antigen-specific T cells in vivo, thereby generating antigen-specific tolerance by targeting the regulatory properties of TREGs to specific antigen targets (p. 6, Results, 1st para, p. 8, Discussion), which would be applicable to controlling the CRS mouse model of Ye in view of Kenderian.
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
Claim 52 is rejected under 35 U.S.C. 103 as being unpatentable over Ye et al., (FASEB J, 2020, 9:12963-12975), in view of Kenderian et al. (US2021/0214723, filed 5/31/2019), as applied to claim 45, in further view of Frank et al. (US2020/0299644, filed 2/08/2018)
As stated supra, Ye in view of Kenderian suggest an irradiated immunodeficient mouse comprising administered human CART cells and PBMCs, and engrafted with a human tumor.
However, Ye and Kenderian are silent with respect to the CART cells being TILs.
Frank teaches compositions for T cell therapy of human tumors comprising administering human TILs comprising an engineered receptor that specifically binds to cell surface antigen on human cancer cells [0023-0024, 0093-0096, 0117-0119, 0292, 0333-0335, 0357-0359, 0402, 0416-0417].
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing to prepare an immunodeficient mouse model comprising administered human CART cells, human PBMCs, and engrafted with a human tumor as taught by Ye in view of Kenderian, and substitute TILs as the CART cells as taught by Frank with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so as taught by Frank because compared to naïve T cells, TILs exhibit increased proliferation, migration, activation and anti-tumor efficacy [0004, 0159].
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
Claims 53 and 57 are rejected under 35 U.S.C. 103 as being unpatentable over Ye et al., (FASEB J, 2020, 9:12963-12975), in view of Kenderian et al. (US2021/0214723, filed 5/31/2019, published 7/15/2021), as applied to claims 45 and 56, in further view of Holland et al. (Cell Tissue Bank, 2018, 19:783790)
As stated supra, Ye in view of Kenderian suggest an irradiated immunodeficient mouse comprising administered human CART cells and PBMCs, and engrafted with a human tumor.
However, although Kenderian teaches the T cells can be obtained from patients to be treated [0049, 0052], they are silent with respect to the PBMCs and tumor cells being autologous.
Holland teaches PBMCs are essential to the study of autoimmune diseases and cancer, and describes compositions of banked human PBMCs from human patients with tumors (Abstract).
Accordingly, it would have been prima facie obvious to one of ordinary skill in the art at the time of filing to prepare an immunodeficient mouse model comprising administered human CART cells, human PBMCs, and engrafted with a human tumor as taught by Kenderian, and choose PBMCs obtained from the human tumor patients as taught by Holland with a reasonable expectation of success. The ordinary skilled artisan would have been motivated to do so not only because Holland suggest using immune cells from the same cancer patient, but as because Holland teaches that in the field of cancer immunology, the cellular phenotyping of a patients PMBCs provides critical information about patients responses to treatments (Abstract/Background, 1st para.), which would be applicable to the CRS mouse model of Ye in view of Kenderian.
Hence, the claimed invention as a whole was prima facie obvious in the absence of evidence to the contrary.
Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory obviousness-type double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); and In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on a nonstatutory double patenting ground provided the conflicting application or patent either is shown to be commonly owned with this application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement.
Effective January 1, 1994, a registered attorney or agent of record may sign a terminal disclaimer. A terminal disclaimer signed by the assignee must fully comply with 37 CFR 3.73(b).
Claims 45-58 are rejected on the grounds of nonstatutory double patenting over claims 1-7 of U.S. Patent No. 12,196,744 (Keck et al., Patented 1/14/2025)
Kenderian et al. (US2021/0214723, filed 5/31/2019, published 7/15/2021).
The subject matter claimed in the instant application is fully disclosed in the referenced patent as follows: the method comprising measure human cytokines uses the immunodeficient mouse of instant application. It is clear that all the elements of the cited patent claims mouse are to bound in instant claims mouse. The difference between the cited patent claims and the instant claims lies in the fact that the cited patent claims are the intended use of instant invention.
Since the instant application claims are obvious over cited patent claims, said claims are not patentably distinct.
Conclusion
No claims are allowed.
Examiner Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to ARTHUR S LEONARD whose telephone number is (571)270-3073. The examiner can normally be reached on Mon-Fri 9am-5pm.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, James Doug Schultz can be reached on 571-272-0763. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
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/ARTHUR S LEONARD/Examiner, Art Unit 1631
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